Research articles
  
ScienceAsia 48 (2022):ID  532-537 |doi: 
						
					10.2306/scienceasia1513-1874.2022.075
  
            
         
          Hedyotis diffusa Willd extract protects rat renal tubular
epithelial cells from high glucose-induced injury by inhibiting
PI3K/AKT signaling pathway
         
          Haiping Donga, Qing Zhangb,*
            
            ABSTRACT:     : The effects of Hedyotis diffusa Willd on high glucose (HG)-induced injury of rat renal tubular epithelial cells
and its related regulatory mechanisms were investigated. In this study, NRK-52E cells were cultured in a normal glucose
concentration (5.5 mM glucose) or HG concentration medium (30 mM glucose), and treated with the concentration
gradient of H. diffusa extract (50, 100, 200 ?g/ml). The results suggested that H. diffusa extract has a protective
effect on the cell viability of NRK-52E cells and inhibited the HG-induced oxidative stress through the detection of
malondialdehyde content and specific activities of superoxide dismutase and glutathione peroxidase. The extract also
inhibited the HG-induced apoptosis. In addition, the epithelial-to-mesenchymal transition (EMT) indicators including
alpha-smooth muscle actin (?-SMA), E-cadherin, N-cadherin and vimentin were measured, it was found that the HGinduced EMT of NRK-52E cells was inhibited by the extract. Moreover, H. diffusa extract exerted an inhibitory effect on
the PI3K/AKT signaling activation induced by HG. Hence, H. diffusa extract could protect rat renal tubular epithelial
cells from HG-induced injury by inhibiting PI3K/AKT signaling pathway.
 
          
                    
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              | a | 
              Department of Endocrinology, Yueqing People?s Hospital, Wenzhou, Zhejiang 325600 China | 
                                     
              | b | 
              Department of Endocrinology, Chongqing Qianjiang Central Hospital, Chongqing 409099 China | 
                                                                                     
                        
                        
                        
            
			            
                        
                        
                       
                      * Corresponding author, E-mail: zhangqing_686@163.com 
          Received 2 Nov 2021, Accepted 24 Feb 2022            
         
        
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